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Type 1 Diabetes in Children

Introduction

Type 1 diabetes is a major problem among young members of the population because they become infringed from their earliest years. Diabetes mellitus (DM) is a large group of complex metabolic diseases characterized by chronic hyperglycemia caused by impaired insulin secretion or action, or a combination of these disorders. Disruption of insulin secretion or a decrease in the response of tissues to insulin as part of complex hormonal processes leads to a disturbance in the effect of insulin on target tissues. The latter causes disorders of carbohydrate, fat, and protein metabolism. The same patient can simultaneously experience a violation of insulin secretion and a violation of its action. Type 1 diabetes is a form of autoimmune disease in genetically predisposed individuals in which chronically occurring lymphocytic insulitis leads to T-cell-mediated β-cell destruction. Subsequently, one can develop absolute insulin deficiency, where one can observe the tendency to develop diabetic ketoacidosis. Although there is a scarcity of data regarding clinical trials and advanced care of type 1 diabetes among children, it is possible to implement prognostics by analyzing their insulin antibodies (IAA) and HbA 1c.

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Literature Review

The general prevalence rate of type 1 diabetes is becoming more prominent among adolescents and children. According to the position statement, there is a significant increase in the occurrence rate among individuals aged 0 through 19 (Chiang et al., 2018). In other words, the problem is on the rise, but there is a lack of sufficient evidence regarding the pediatric aspect of advanced care. There is an evident scarcity in clinical trials among children and adolescents, which makes it more challenging to handle issues in a proper manner (Chiang et al., 2018). Autoimmune diabetes is characterized by the destruction of ß-cells, the presence of autoantibodies, absolute insulin deficiency, and complete insulin dependence.

The main reason for most of the manifestations of diabetes mellitus is the absolute deficiency of insulin in the case of type 1 diabetes mellitus. In addition, it may have insufficient action or inadequate secretion, as well as the lowered response of the hormone in the periphery. Due to the lack of insulin, there is insufficient use of glucose by insulin-dependent tissues, primarily the liver, muscle, and fat. Whereas in insulin-independent tissues, the polyol pathway of glucose utilization is activated with the formation of highly osmotic compounds of sorbitol and fructose. Due to an acute insulin deficiency, a state of energy hunger develops in the body. It manifests itself in a violation of the transport of glucose from the peripheral vascular bed to the cells of insulin-dependent tissues. This occurs due to catabolic processes aimed at resolving the created energy problem.

In addition, there is a severe course with a tendency for diabetic ketoacidosis, an association with genes of the major histocompatibility complex. Idiopathic diabetes also occurs with β-cell destruction and a propensity for diabetic ketoacidosis. However, this happens without signs of an autoimmune process of specific autoantibodies and association with the system. Type 1 diabetes mellitus is characterized by chronic, immune-mediated destruction of ß-cells of the islets of the pancreas, which in most cases leads to absolute insulin deficiency. The damage of β-cells occurs at different rates and becomes clinically significant when approximately 90% of the β-cells are destroyed (Holt, Cockram, Flyvbjerg, & Goldstein, 2017). DM 1 is a multifactorial disease, however, the specific mechanisms of interaction between genetic predisposition, environmental factors, and the state of the immune system that underlie DM 1 remain unclear.

Autoimmune destruction of ß-cells is a complex, multi-stage process, during which both the cellular and humoral links of immunity are activated. The first to infiltrate the islets of Langerhans are monocytes and macrophages, which secrete pro-inflammatory cytokines and free radicals of oxygen, nitric oxide, hydroxyl radicals. Cytokines induce apoptosis – the programmed death of transformed or healthy cells, and nitric oxide and other radicals damage deoxyribonucleic acid of ß-cells (Holt et al., 2017). Given the low antioxidant enzymatic protection of ß-cells, free radicals cause denaturation of proteins with the destruction of ß-cells. T-lymphocytes activated by pro-inflammatory cytokines recognize denatured proteins and other products of β-cell damage as antigens and are included in the insulitis formation.

Autoantibodies linked with type 1 diabetes are serological markers of autoimmune elimination of ß-cells. These include antibodies to glutamate decarboxylase (GADA), tyrosine phosphatase (IA2), insulin (IAA), and zinc transporter 8 (ZnT8A) (Endesfelder et al., 2018). There is an age-related dissociation in the appearance of these antibodies, where IAA and GADA are more often expressed in children under the age of 10, while IA2 and ZnT8A are more often shown at an older age. It is stated that there is a higher risk of DM 1 progression among children who developed IAA and IA-2A (Endesfelder et al., 2018). In addition, HbA 1c levels also can act as a strong predictor of the diagnosis of type 1 diabetes among children (Helminen et al., 2015). The value of anti-islet antibodies both in predicting type 1 diabetes and in differential diagnosis with other types of diabetes has decreased with the emergence of stronger markers.

Analysis

Based on the current literature, one can outline the stages of development of type 1 diabetes among children. The disease is an inextricable process that sequentially progresses through various identifiable stages until the onset of clinical symptoms, which made it possible to distinguish several stages of type 1 diabetes. Phase one is an autoimmune process that is characterized by the absence of clinical manifestations. Here there is a presence of signs of a β-cell autoimmune process, determined by the prevalence of several positive titer marks of autoantibodies. At the same time, glycemic indicators do not exceed the norm, and there are no clinical manifestations of diabetes. The duration of the first stage can be months or years (Holt et al., 2017). At the second stage of diabetes mellitus 1, disorders of carbohydrate metabolism join the signs of a β-cell autoimmune process.

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The third stage is the onset of type 1 diabetes with the classic clinical presentation. These might include weight loss, polydipsia, and polyuria (Holt et al., 2017). Stage four is established diabetes, and many children with type 1 diabetes mellitus may experience partial remission of DM 1 soon after starting insulin therapy. The latter lasts from several weeks to six months, but remission of diabetes mellitus is temporary and does not mean a cure for diabetes. Complete remission is the cessation of insulin administration without worsening glycemic parameters.

Doses of insulin preparations and the scheme of administration are selected individually for each patient based on age, insulin action profile, and individual tolerance based on glycemic control data. Doses of insulin preparations and the scheme of their administration can vary significantly between patients with type 1 diabetes, including during the period of remission, doses of insulin preparations may be minimal, up to complete cancellation for a certain time. However, the final decision on the scheme and prescriptions depends strictly on the glycemic parameters and level HbA 1c. Patients or legal representatives should be advised to record data in self-control diaries indicating the date and time of blood glucose levels, insulin doses, carbohydrates taken, episodes of hypo- and hyperglycemia and other conditions (Holt et al., 2017). Self-monitoring data should be regularly analyzed by patients and parents, and are also necessary during visits to the attending physician for the timely assessment and correction of the treatment.

Dietary recommendations should be based on healthy eating principles and appropriate for all children, adolescents with type 1 diabetes, and their families to improve the results of diabetes control and reduce cardiovascular risks. Nutritional guidelines should be culturally, ethnically, and individually adapted and take into account the cognitive and psychosocial aspects of the child and family (Holt et al., 2017). Nutritional advice should be provided to the patient when managing both regular and unforeseen physical activity, and to achieve individual goals in competitive sports.

Conclusion

In conclusion, the current prevalence of type 1 diabetes among children is a major concern that needs to be addressed by increasing the current understanding of the issue. Although there are some data regarding the antibodies and prognostic approaches, one can observe the scarcity of clinical trials and developments regarding advanced care for the target population. Such care can be developed by regularly testing children for the presence of insulin antibodies and HbA 1c. In addition, the staging process allows the clinicians to properly assess a patient’s progression stage.

References

Chiang, J. L., Maahs, D. M., Garvey, K. C., Hood, K. K., Laffel, L. M., Weinzimer, S. A., … Schatz, D. (2018). Type 1 diabetes in children and adolescents: A position statement by the American Diabetes Association. Diabetes Care, 41(9), 2026-2044. Web.

Endesfelder, D., Castell, W. zu, Bonifacio, E., Rewers, M., Hagopian, W. A., … She, J. (2018). Time-resolved autoantibody profiling facilitates stratification of preclinical type 1 diabetes in children. Diabetes, 1, 1-38. Web.

Helminen, O., Aspholm, S., Pokka, T., Hautakangas, M.-R., Haatanen, N., Lempainen, J., … Veijola, R. (2015). HbA1c predicts time to diagnosis of type 1 diabetes in children at risk. Diabetes, 64(5), 1719-1727. Web.

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Holt, R. I. G., Cockram, C., Flyvbjerg, A., & Goldstein, B. J. (Eds.). (2017). Textbook of diabetes. Hoboken, NJ: Wiley-Blackwell.

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